The release of energy from foods and food products is a complex process. It depends on the composition, structure, extent of modification and volume of the food. Apart from this, it is also variable between individuals and reflects many different factors which probably include a combination of age, level of fitness, rate of gastric emptying and peristalsis, sex, size, state of health etc. Energy may be derived from different food sources, for example, carbohydrates, lipids and proteins, alcohol etc. In many animals, including man, energy is stored as fat (adipose tissue) and provides a reserve when food is limiting. There is a more readily available form of energy, however, where a glucose polymer (glycogen) is stored in muscles and the liver and can be rapidly mobilised when required. The formation and storage of glycogen is a synchronised enzymatic process which is controlled in part by insulin which promotes the formation of glycogen from the glucose precursors (FIG. 1). Glucose deposition and glycogen catabolism is co-ordinated in man to maintain blood glucose at ˜4.5 mmol l−1.
Glycogen Storage Disease
In the normal human, the anabolism and catabolism of glycogen is normally co-ordinated and regulated. The deposition of glycogen is promoted by insulin whilst the hydrolysis of glycogen and conversion to glucose is promoted by adrenaline (especially muscle) and glucagons (especially liver).
In glycogen storage disease (GSD) there is an inherited defect with respect to the deposition or hydrolysis of glycogen (http<<colon>>//www<<dot>>agsd<<dot>>org<<dot>>uk/home/information<<dot>>asp>; http<<colon>>//agsdus<<dot>>org/body_whatis—1<<dot>>html) and consequently the concentration of blood glucose. FIG. 1 outlines the principles of glycogen metabolism.
The most common types of glycogen storage disease are:                In Type I (Von Gierke Disease) individuals suffer from a lack of glucose-6-phosphatase activity (‘h’ in FIG. 1) and hence cannot generate glucose from glycogen. Consequently they need to be tube fed to maintain blood glucose.        In Type II (Pompe's Disease) individuals suffer from a lack of α-glucosidase activity (‘i’ in FIG. 1). Infants often die of this form very young.        In Type III (Cori's Disease) individuals suffer from a lack of debranching enzyme activity (‘i’ in FIG. 1). Treatment usually consists of a high protein diet.        In Type IV (Anderson's Disease) individuals suffer from a lack of branching enzyme activity (‘e’ in FIG. 1). Liver transplantation is the only viable therapy.        In Type V (McArdle's Disease) individuals suffer from a lack of muscle phosphorylase activity (‘f’ in FIG. 1). Extensive exercise should be avoided.        In Type VI (Her's Disease) individuals suffer from a lack of liver phosphorylase activity (‘f’ in FIG. 1). There is a male X-chromosome link.        In Type VII (Tarui's Disease) individuals suffer from a lack of muscle phosphofructokinase activity. Extensive exercise should be avoided.        In Type IX individuals suffer from a lack of liver phosphorylase activity (‘f’ in FIG. 1). There is a male X-chromosome link and it is comparable to type VI.        
Low blood glucose can be treated by the slow administration of glucose (oral or intravenous), or from starch hydrolysates (e.g. maltose, dextrins etc.) or from native starch where glucose is liberated as a consequence of digestion. In practice ‘corn-starch’, which is normal maize starch, is used to treat glycogen storage disease (especially during sleep) due to availability and to lack of a superior alternative in terms of digestive response. The starch must be slowly digested and not converted to glucose rapidly or excreted with little hydrolysis. In other clinical conditions (such as diabetes mellitus) there is also the need to supply glucose slowly and from a non-sugar based matrix (e.g. cakes, biscuits, sweets etc.). This can, therefore, also be achieved by starch (hydrolysis in the gut) and is important for night time regimes where glucose is essential in the blood but within a controlled form.
The advantages and disadvantages of feeding glucose, maltodextrins or maize starch for clinical nutrition with a perceived optimal substrate are defined in Table 1.
TABLE 1Release profile of glucose based substrates in the gutof man with perceived optimised product in this respectNormal maizeEntry toMalto-(‘corn’)bodyGlucosedextrinstarchIntravenousUsedToo highInappropriateAppropriateextensivelymolecularin view ofin view ofin medicine.weightsize,size,Would needcompositioncompositionto be pumpedandandconstantlystructurestructurefor GSD anddiabetesclinicalmaintenance.Oral - smallRapidlyRapidlyGlucoseGlucoseintestineabsorbedabsorbedreleasedreleased(1.5 hours)(1.5within 4over 7.5hours)hourshours (toprovideovernightrelease)Oral - largeNotNotPossiblyMinimalintestineapplicableappli-mostlyfermentablecabledigestedsubstrate towith smallavoid lossamount ofof energyfermentableandsubstratefermentationSlow Release of Energy
Apart for the clinical conditions described above, athletes require sustained release of energy. There are many products on the market which release energy based on sugars or maltodextrins. These include products presented in Table 2. However, sugars and dextrins are absorbed very rapidly and these products must be consumed regularly to maintain the required body loading of the energy.
TABLE 2Energy based products currently found on the market.Carbohydrate,Carbohydrates usedProduct% of productas energy sourceAccelerade7.75Fructose, maltodextrin and sucroseAllsport9.00High fructose syrupCytomax6.00High fructose syrup and maltodextrinEnervit G7.60Fructose, glucose, maltodextrinand sucroseExtran5.00Fructose and maltodextrinthirstquencherG Push7.50Fructose, galactose and maltodextrinGatorade6.00Fructose, glucose and sucroseGU205.70Fructose and maltodextrinPowerade8.00High fructose syrup andglucose polymers [sic]Revenge Sport7.00Fructose, glucose and maltodextrin(adapted from www<<dot>>accelerade<<dot>>com/accelerade-comparison-results<<dot>>asp)Slow Energy Release Nutritional Formulations
As mentioned above, slow release products for sports nutrition tend to be pouched relying on glucose or maltodextrin to supply the energy. These actually are absorbed quickly as they are either readily absorbed (e.g. glucose) or converted to glucose relatively rapidly (e.g. maltodextrins, probably within 60 minutes maximum).
On the other hand, glycogen storage disease (certain treatable forms, see above) management requires that patients receive a slow release of glucose, especially, for example, overnight. Native starch is provided for this purpose where: the initial liberation phase of glucose is not too rapid (see figures below); glucose is released at as constant a rate as possible which must not be too slow or too fast and; the production of lactate (anaerobic respiration) is minimised. Certain starches are to be avoided as they exhibit only limited hydrolysis in the native form (e.g. potato).
Hence, the extent and rate of starch digestion are important parameters with respect to glucose release from the ingested α-glucan. Regulation in terms of these parameters reflect the state of the starch and the rate at which the energy source travels through the gut. A balance in terms of energy release is required which can be controlled by the energy source and the transit time.
Osmolality is also an important feature with respect to carbohydrate usage. Sugar solutions exert a high osmotic pressure compared to polysaccharides due to the number of moles in solution.
The viscosity of the consumed material will also affect the capacity for it to be hydrolysed and to permit associated compounds to come into contact with the mucosal surface. This is a very important issue with respect to product development regarding potential energy sources.
Glycaemic Index (GI) is also an important determinant of energy availability from foods and more especially α-glucans. In this context, white bread has a GI of 1 which is the same as pure glucose and represents one hundred percent availability of the α-glucan fraction (or 1 on a scale from 0 to 1).
Gastric Emptying
As mentioned above, the rate and extent of gastric emptying will in part regulate the transit time of food materials through the gut. It is established that high volumes—low energy promote gastric emptying whereas low volumes—high energy restrict gastric emptying. Lipids and proteins are valuable aids with respect to restricting emptying of the stomach.
Glycogen storage disease and diabetes are classically managed by feeding ‘cornstarch’ which is normal maize starch (Kaufman, 2002). Sometimes, proportions of carbohydrates are utilised which provide rapid (e.g. sugar), medium (e.g. gelatinised starch) and slow (‘cornstarch’) digestion and hence glucose appearance in the blood (Wilbert, 1998). Sugar combinations with or without maltodextrins or ‘glucose polymers’ are often employed in ‘energy drinks’ (including rehydration drinks) and often with other components like salts, protein, fatty acids, glycerol, minerals, flavouring etc. (Gawen, 1981; Tauder et al, 1986; Burling et al, 1989; Gordeladze, 1997; Paul and Ashmead, 1993 and 1994; Vinci et al, 1993; Fischer et al, 1994; Simone, 1995; Gordeladze, 1997; King, 1998; Kurppa, 1998; Cooper et al, 2001; Portman, 2002). The maltodextrins/glucose polymers are used to slow energy availability (compared to sugars) and exert less osmotic pressure.
Brynolf et al (1999) describe the production of an acid modified starch with a molecular weight of 15,000 to 10,000,000 produced by classical acid hydrolysis of starch to be used as an energy source prior to physical activity. Lapré et al (1996) have discussed the option of coating food with non-starch polysaccharides (cation gelling) to reduce the glycaemic response of carbohydrate containing foods.
However, although currently available starch preparations used in the treatment of conditions such as GSD have prolonged glucose release profiles compared to glucose and maltodextrin based products, the time period over which the products enable serum glucose levels to be maintained within an acceptable range is relatively short. Thus, at present, using conventional oral preparations, patients susceptible to hypoglycaemic episodes generally must ingest such glucose sources at intervals of no longer than 4 hours. Although this may be acceptable during daytime, the need for repeated feeding is very inconvenient at nighttime. The patient thus must either awake or be wakened overnight to feed or, alternatively, sleep with a nasogastric tube in place to provide a constant source of glucose.
Accordingly, there is a great need for alternative means of maintaining serum glucose levels within safe ranges over a longer period of time than that afforded by the conventional treatments.